title: Concurrent compliance reduction and increased peripheral resistance in the manifestation of isolated systolic hypertension.
abstract: The hemodynamic mechanisms responsible for producing isolated systolic hypertension (ISH) in the elderly are generally attributed to a decrease in arterial compliance. However, no consistent theoretical or experimental model has been proposed for the production of ISH. This problem was investigated with the use of computer simulation of the modified Windkessel model, an often-used tool in the study of arterioventricular function. Aortic pressure (Pa(t] and aortic flow (Qa(t] data were used to obtain the model parameters: peripheral resistance (Rs), arterial compliance (C) and characteristic impedance of the proximal aorta (Zo). Using Qa(t) as the input to the model, the effects of altered vascular properties on Pa(t) were studied by changing these model parameters. Graded reductions of C (25, 50 and 75%) alone increased systolic pressure (Ps), but also decreased diastolic pressure (Pd) to values below those found in ISH. On the other hand, an increase in Rs of 25% along with a 50 to 75% increase in C resulted in percent changes in Ps and Pd that would result in ISH from a normal pressure level. These results were consistent for a wide range of pressures. Decreased arterial compliance alone is not always responsible for the production of ISH. Rather, isolated systolic hypertension is usually the result of greatly reduced arterial compliance along with a smaller but significant increase in peripheral resistance.
authors.affiliation: Department of Biomedical Engineering, Rutgers University, Piscataway, New Jersey 08855-0909.
authors.forename: D S
authors.initials: DS
authors.lastname: Berger
authors.forename: J K
authors.initials: JK
authors.lastname: Li
mesh_terms: D000368:Aged; D000818:Animals; D003198:Computer Simulation; D004285:Dogs; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D008955:Models, Cardiovascular; D013599:Systole; D014655:Vascular Resistance / Q000502:physiology*